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Long Term Evolution of Glucocorticoid-Suppressible Hyperaldosteronism^*

Ewen Downie Metabolic Unit and Monash University Department of Medicine, Alfred Hospital, and the Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne Melbourne, Victoria, Australia

Address all correspondence and requests for reprints to: J. R. Stockigt, M.D., Ewen Downie Metabolic Unit, Alfred Hospital, Commercial Road, Melbourne, Victoria, Australia 3181.

It is generally held that idiopathic hyperaldos-teronism and glucocorticoid-suppressible hyperaldosteronism (GSH) are distinct entities, distinguishable by thorough investigation. We report a patient who presented in 1974 at age 15 yr with blood pressure of 240/120 mm Hg, serum K of 3.1 mM, low renin, and high normal aldosterone excretion, with findings diagnostic of GSH. After dexamethasone treatment (2 mg/day for 4 weeks), urinary aldosterone was undetectable (<1 µg/24 h), associated with correction of hypertension and hypokalaemia. While untreated, plasma aldosterone increased in response to ACTH infusion at a dose that did not influence plasma cortisol. Plasma aldosterone at 0800 h while recumbent was higher than in subsequent samples taken while ambulant, consistent with ACTH dependence of aldosterone secretion. Blood pressure, renin, and potassium remained normal for 4 yr during treatment, with dexamethasone (0.5–0.75 mg/day), but hypertension then slowly returned. After 7 yr, the original studies were repeated. Urinary aldosterone excretion was again in the high normal range after 3 weeks of no treatment, but both plasma renin and aldosterone consistently increased in response to upright posture. After dexamethasone treatment (2 mg/day) for 4 weeks, urinary aldosterone was not suppressed (excretion rate, 10.8, 9.2, and 5.7 µg/day; urinary Na, >100 mmol/day; urinary cortisol, <1 µg/day). At this time, dexamethasone did not alleviate hypertension or increase renin. Control of blood pressure has been readily achieved, 8–12 yr after diagnosis, with a low dose of β-adrenergic antagonist and amiloride. Aldosterone remains incompletely suppressible during sodium loading, so that the findings now resemble those of idiopathic hyperaldosteron-ism. This sequence indicates that glucocorticoids may not per--manently control hypertension in GSH. The transient dominance of ACTH in control of aldosterone secretion indicates that the relationship between GSH and idiopathic hyperaldos-teronism merits further evaluation in long term studies.

^* This work was supported by the National Health and Medical Research Council of Australia and the National Heart Foundation. Presented in part at Seventh Asia and Oceania Congress of Endocrinology, Tokyo, Japan, September 1982.

Received May 19, 1986.

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